This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Synaptic growth and function of the Drosophila larva neuromuscular junction (NMJ) requires retrograde signaling mediated by muscle-derived Bone Morphogenetic Proteins (BMPs) and neuronal BMP receptors. How signaling at the synaptic terminal is relayed to the cell body and nucleus to regulate transcription is unknown. We find that the type I receptor Thick veins (Tkv) and the type II receptor Wishful thinking (Wit) localize in punctate structures at the NMJ synaptic boutons, axons, and cell body of motoneurons. Both receptors traffic anterogradely and retrogradely in motoneurons axons;and impairment of receptor traffic correlates with a decrease in signaling through the pathway. In addition to anterograde and retrograde traffic of type I and type II receptors independently of each other, we also detect retrograde co-localized vesicular traffic of Tkv and Wit. This co-localized retrograde traffic of Wit and Tkv is disrupted in gbb mutants where the signaling pathway is inactive, and the type II receptor Wit is down regulated. We propose that co-localized receptor traffic constitutes a complex of the activated receptors in a BMP signaling endosome and that similar to neurotrophins, this BMP signaling endosome relays the Gbb signal from the synaptic terminal to the cell body to activate downstream effectors and transcription of genes required for synaptic growth. The goal of the experiments to be performed at LSF is to detect the interaction of Wit and Tkv in endosomes by FLIM-based FRET.